DNA repair gene polymorphisms at XRCC1, XRCC3, XPD, and OGG1 loci in Maharashtrian population of central India

Reduction in DNA repair capacity is associated with increased rates of birth defects, cancer, and accelerated ageing. Genetic polymorphisms in DNA repair genes might influence the repair activities of the enzymes predisposing individuals to cancer risk. Owing to the presence of these genetic variants, inter-individual and ethnic differences in DNA repair capacity have been observed in various populations. India harbors enormous genetic, cultural and linguistic diversity. The present study was undertaken to determine the allele and genotype frequencies of four non-synonymous SNPs, XRCC1 Arg399Gln (C > T, rs25487), XRCC3 Thr241Met (G > A, rs861539), XPD Lys751Gln (T > G, rs13181), and OGG1 Ser326Cys (C > G, rs1052133) in the Maharashtrian population, residing in the Vidarbha region of central India and to compare them with HapMap and other Indian populations. The variant alleles of these polymorphisms have been found to be positively associated with different forms of cancer in several genetic epidemiological studies. The basic prevalence of these polymorphisms in the general population must be known to evaluate their significance in risk assessment in cancer and other phenotypes. About 215 healthy and unrelated individuals from the Maharashtrian population were genotyped for each of these four polymorphisms using PCR-RFLP. The allele and genotype frequency distribution at the four DNA repair gene loci among Maharashtrians revealed a characteristic pattern. To the best of our knowledge, this is the first report of these DNA repair gene polymorphisms in a central Indian population.     

Assessment of DNA damage in Brazilian workers occupationally exposed to pesticides: a study from Central Brazil

We evaluated 41 rural workers occupationally exposed to pesticides and 32 subjects as a control group, using the micronucleus (MN) and the comet assay. For the comet assay, we evaluated the peripheral blood, and for the MN, we sampled cells from the oral epithelium. Damage to DNA was measured by tail length, % DNA in tail (% tail), olive tail moment (OTM), and tail moment (TM). The exposed group presented an 8× increase in MN frequency, when compared to the control group (p <0.05). When we contrasted the MN frequencies between the individuals that use and do not use personal protective equipment, we found a mean of 7.5 MN (57 % variance) and 12.1 MN (130 % variance), respectively. The binucleated cells were 0.04 and 0.005, in the exposed and control groups, respectively, indicating 8× increase in the number of binucleated cells, when comparing the groups (p <0.05). In the comet assay, we demonstrated statistically significant differences in three parameters (% DNA, OTM, and TM) indicating that the rural workers presented high levels of genomic damages. Our results indicate that occupational exposure to pesticides could cause genome damage in somatic cells, representing a potential health risk to Brazilian rural workers that deal constantly with agrochemicals without adequate personal protection equipment.     

Cypermethrin has the potential to induce hepatic oxidative stress, DNA damage and apoptosis in adult zebrafish (Danio rerio)

Cypermethrin (CYP), a widely used Type II pyrethroid pesticide, is one of the most common contaminants in the freshwater aquatic system. We studied the effects of CYP exposure on the induction of hepatic oxidative stress, DNA damage and the alteration of gene expression related to apoptosis in adult zebrafish. Hepatic mRNA levels for the genes encoding antioxidant proteins, such as Cu/Zn-Sod, Mn-Sod, Cat, and Gpx, were significantly upregulated when zebrafish were exposed to various concentrations of CYP for 4 or 8 days. In addition, the main genes related to fatty acid β-oxidation and the mitochondrial genes related to respiration and ATP synthesis were also significantly upregulated after exposure to high concentrations (1 and 3 μg L⁻¹) of CYP for 4 or 8 days. Moreover, in a comet assay of zebrafish hepatocytes, tail DNA, tail length, tail moment and Olive tail moment increased in a concentration-dependent manner. The significant induction (p < 0.01) of all four parameters observed with CYP concentrations of 0.3 μg L⁻¹ or higher suggests that heavy DNA damage was induced even at low levels. Furthermore, several apoptosis- related genes, such as p53, Apaf1 and Cas3, were significantly upregulated after CYP exposure, and Bcl2/Bax expression ratio decreased, especially in groups treated with 1 and 3 μg L⁻¹ CYP for 8 days. Taken together, our results suggested that CYP has the potential to induce hepatic oxidative stress, DNA damage and apoptosis in zebrafish. This information will be helpful in fully understanding the mechanism of aquatic toxicology induced by CYP in fish.     

Atrazine promotes biochemical changes and DNA damage in a Neotropical fish species

The effects of Atrazine, an herbicide used worldwide and considered as a potential contaminant in aquatic environments, were assessed on the Neotropical fish Prochilodus lineatus acutely (24 and 48 h) exposed to 2 or 10 μg L⁻¹ of atrazine by using a set of biochemical and genetic biomarkers. The following parameters were measured in the liver: activity of the biotransformation enzymes ethoxyresorufin-O-deethylase (EROD) and glutathione S transferase (GST), antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), content of reduced glutathione (GSH), generation of reactive oxygen species (ROS) and occurrence of lipid peroxidation (LPO); in brain and muscle the activity of acetylcholinesterase (AChE) and DNA damage (comet assay) on erythrocytes, gills and liver cells. A general decreasing trend on the biotransformation and antioxidant enzymes was observed in the liver of P. lineatus exposed to atrazine; except for GR, all the other antioxidant enzymes (SOD, CAT and GPx) and biotransformation enzymes (EROD and GST) showed inhibited activity. Changes in muscle or brain AChE were not detected. DNA damage was observed in the different cell types of fish exposed to the herbicide, and it was probably not from oxidative origin, since no increase in ROS generation and LPO was detected in the liver. These results show that atrazine behaves as enzyme inhibitor, impairing hepatic metabolism, and produces genotoxic damage to different cell types of P. lineatus.     

Assessment of DNA damage and cholinesterase activity in soybean farmers in southern Brazil: High versus low pesticide exposure

Abstract

The aim of this study was to evaluate the DNA damage in soybean growers during two agricultural periods of a crop season (high and low exposure) and a control group, as well as butyrylcholinesterase (BChE) activity during these exposure periods in order to estimate the degree of BChE inhibition for the exposed group. DNA damage in peripheral whole blood was evaluated by the comet assay and plasma BChE activity was accessed as a measure of exposure to cholinesterase inhibitors. None of the soybean growers reported using full Personal Protective Equipment (PPE). BChE was lower in high exposure period than in low exposure period and DNA damage index was significantly increased in the high exposure period than in the low exposure period. In addition, DNA damage in both exposure periods was higher than control group. No correlation was found between exposure time and DNA damage and BChE activity. However, negative correlation was observed between DNA damage in high and low exposure periods. The results indicate that soybean growers are exposed to cholinesterase inhibitors and to pesticides mixtures with genotoxic potential.     

DNA damage effect of cyprodinil and thiacloprid in adult zebrafish gills

Cyprodinil and thiacloprid are two of the most commonly used pesticides in Turkey. It is more likely to reach humans or animals due to their widespread use. This study aims to investigate whether there is a DNA damage risk due to cyprodinil and thiacloprid exposure. Zebrafish, which is used as a model organism in health and environmental research, and comet assay were chosen to demonstrate this damage. Ten zebrafish per group were exposed to 2 different concentrations for each pesticides (0.31 and 0.155 mg/L for cyprodinil and 1.64 and 0.82 mg/L for thiacloprid) for 21 days. After, gills were excised and comet assay was performed. Photos of an average of 50 cells per slide were taken and were analyzed with visual evaluation program. DNA damage was found to be increased in the 0.31 mg/L cyprodinil, 0.82 mg/L thiacloprid, and 1.64 mg/L thiacloprid treatment groups when compared to the control group (p < 0.001). Average tail DNA percentage parameter values were 9.45 ± 0.51, 10.30 ± 0.34, 11.17 ± 0.33, and 2.47 ± 0.06 respectively. Cyprodinil and thiacloprid were identified as genotoxic agents that should be investigated further.

     

DNA damage and repair process in earthworm after in-vivo and in vitro exposure to soils irrigated by wastewaters

In this study, DNA damage to earthworms (Eisenia fetida) after in vivo exposure to contaminated soils was measured by detecting DNA strand breakages (DSBs) and causality was analyzed through fractionation based bioassays. A non-linear dose-response relationship existed between DNA damage and total soil PAHs levels. DNA damage, measured with the comet assay, and its repair process, were observed. To identify the chemical causality, an in vitro comet assay using coelomocytes was subsequently performed on the fractionated organic extracts from soils. The results showed that the PAHs in the soils were responsible for the exerting genotoxic effects on earthworms. When normalized to benzo(a)pyrene toxic equivalent (TEQ(BaP)), the saturation dose in the dose-response curve was about 10ng TEQ(BaP) g(-1) soil (dw).     

Use of sensitive methods for detection of DNA damage on human lymphocytes exposed to p,p′-DDT: Comet assay and new criteria for scoring micronucleus test

Wide distribution, stability and long persistence in the environment of dichlorodiphenyltrichloroethane (DDT), probably the best-known and most useful insecticide in the world, imposes the need for further examination of the effect of this chemical on human health and especially on the human genome. In this study, peripheral blood human lymphocytes from a healthy donor were exposed to 0.025 mg/L concentration of p,p′-DDT at different time periods (1, 2, 24 and 48 h). For the assessment of genotoxic effect, the new criteria for scoring micronucleus test and alkaline comet assay were used. Both methods showed that p,p′-DDT induces DNA damage in low concentration used in this research. Results of micronucleus test showed a statistically significant (p < 0.05) genotoxic effect of p,p′-DDT on human lymphocytes compared with corresponding control and a different exposure time. A comet assay also showed increased DNA damage caused in p,p′-DDT-exposed human lymphocytes than in corresponding control cells for the tail length. Results obtained by measuring the level of DNA migration and incidence of micronuclei (MN), nucleoplasmic bridges (NPBs) and nuclear buds (NBUDs) indicate the sensitivity of these tests and their application in detection of primary genome damage after long-term exposure to establish the effect of p,p′-DDT on human genome.     

Cytogenetic status of human lymphocytes after exposure to low concentrations of p,p'-DDT, and its metabolites (p,p'-DDE, and p,p'-DDD) in vitro

Despite that the use of DDT has been restricted for more than 40 years to malaria affected areas, low doses of this pesticide and its metabolites DDE and DDD can be found in the environment around the world. Although it has been shown that these pollutants induce cell and DNA damage, the mechanisms of their cytogenotoxic activity remains largely unknown. This study looks into their possible genotoxic effects, at doses that can be found in body fluids, on human lymphocytes using the cytokinesis-block micronucleus assay and the comet assay. After exposure for 1, 6, and 24 h compounds p,p′-DDT (0.1 μg mL⁻¹), p,p′-DDE (4.1 μg mL⁻¹), and p,p′-DDD (3.9 μg mL⁻¹) showed increase in DNA damage. The most significant results were observed at exposure period of 24 h where number of micronucleated cells increased from control 2.5 ± 0.71 to 23.5 ± 3.54, 13.5 ± 0.71, and 16.5 ± 6.36 for DDT, DDE, and DDD, respectively. Similar effect was observed using comet test where the percentage of DNA in comets tail increased from control 1.81 ± 0.16 to 17.24 ± 0.55, 11.21 ± 0.56 and 9.28 ± 0.50 for each compound, respectively. At the same time Fpg-comet assay failed to report induction of oxidative DNA damage of these pollutants. Additionally, the type of cell death was determined using diffusion assay and necrosis dominated. Our findings suggest that even at low concentrations, these pesticides could induce cytogenetic damage to human peripheral blood lymphocytes and in that manner have the impact on human health as well.     

DNA damage in Populus tremuloides clones exposed to elevated O3

The effects of elevated concentrations of atmospheric tropospheric ozone (O₃) on DNA damage in five trembling aspen (Populus tremuloides Michx.) clones growing in a free-air enrichment experiment in the presence and absence of elevated concentrations of carbon dioxide (CO₂) were examined. Growing season mean hourly O₃ concentrations were 36.3 and 47.3 ppb for ambient and elevated O₃ plots, respectively. The 4th highest daily maximum 8-h ambient and elevated O₃ concentrations were 79 and 89 ppb, respectively. Elevated CO₂ averaged 524 ppm (+150 ppm) over the growing season. Exposure to O₃ and CO₂ in combination with O₃ increased DNA damage levels above background as measured by the comet assay. Ozone-tolerant clones 271 and 8L showed the highest levels of DNA damage under elevated O₃ compared with ambient air; whereas less tolerant clone 216 and sensitive clones 42E and 259 had comparably lower levels of DNA damage with no significant differences between elevated O₃ and ambient air. Clone 8L was demonstrated to have the highest level of excision DNA repair. In addition, clone 271 had the highest level of oxidative damage as measured by lipid peroxidation. The results suggest that variation in cellular responses to DNA damage between aspen clones may contribute to O₃ tolerance or sensitivity.     

Use of sensitive methods for detection of DNA damage on human lymphocytes exposed to p,p'-DDT: Comet assay and new criteria for scoring micronucleus test

Wide distribution, stability and long persistence in the environment of dichlorodiphenyltrichloroethane (DDT), probably the best-known and most useful insecticide in the world, imposes the need for further examination of the effect of this chemical on human health and especially on the human genome. In this study, peripheral blood human lymphocytes from a healthy donor were exposed to 0.025 mg/L concentration of p,p'-DDT at different time periods (1, 2, 24 and 48 h). For the assessment of genotoxic effect, the new criteria for scoring micronucleus test and alkaline comet assay were used. Both methods showed that p,p'-DDT induces DNA damage in low concentration used in this research. Results of micronucleus test showed a statistically significant (p < 0.05) genotoxic effect of p,p'-DDT on human lymphocytes compared with corresponding control and a different exposure time. A comet assay also showed increased DNA damage caused in p,p'-DDT-exposed human lymphocytes than in corresponding control cells for the tail length. Results obtained by measuring the level of DNA migration and incidence of micronuclei (MN), nucleoplasmic bridges (NPBs) and nuclear buds (NBUDs) indicate the sensitivity of these tests and their application in detection of primary genome damage after long-term exposure to establish the effect of p,p'-DDT on human genome.     

Evaluation of copper-induced DNA damage in Vitis vinifera L. using Comet-FISH

The contamination of soils and water with copper (Cu) can compromise the crops production and quality. Fungicides containing Cu are widely and intensively used in viticulture contributing to environmental contamination and genotoxicity in Vitis vinifera L. Despite the difficulty in reproducing field conditions in the laboratory, hydroponic solutions enriched with Cu (1, 10, 25 and 50 μM) were used in forced V. vinifera cuttings to evaluate the DNA damage in leaves of four wine-producing varieties (‘Tinta Barroca’, ‘Tinto Cão’, ‘Malvasia Fina’ and ‘Viosinho’). Alkaline comet assay followed by fluorescence in situ hybridisation (Comet-FISH) was performed with the 45S ribosomal DNA (rDNA) and telomeric [(TTTAGGG)_n] sequences as probes. This study aimed to evaluate the tolerance of the four varieties to different concentrations of Cu and to determine which genomic regions were more prone to DNA damage. The comet assay revealed comets of categories 0 to 4 in all varieties. The DNA damage increased significantly (p < 0.001) with the Cu concentration. ‘Tinto Cão’ appeared to be the most sensitive variety because it had the highest DNA damage increase in 50 μM Cu relative to the control. Comet-FISH was only performed on slides of the control and 50 μM Cu treatments. Comets of all varieties treated with 50 μM Cu showed rDNA hybridisation on the head, ‘halo’ and tail (category III), and their frequency was significantly higher than that of control. The frequency of category III comets hybridised with the telomeric probe was only significantly different from the control in ‘Malvasia Fina’ and ‘Tinta Barroca’. Comet-FISH revealed partial damage on rDNA and telomeric DNA in response to Cu but also in control, confirming the high sensitivity of these genomic regions to DNA fragmentation.

     

Impact of the toxicity of Cylindrospermopsis raciborskii (Woloszynska) Seenayya & Subba Raju on laboratory rats in vivo

In vivo laboratory studies of toxicity were performed on Wistar rats using a methanol extract produced by the natural population of Cylindrospermopsis raciborskii (abundance of 2.13 × 10⁵ trichomes mL⁻¹) collected at Aleksandrovac Lake (Serbia). HPLC analysis showed that the extract contains 6.65 μg cylindrospermopsin (CYN) mg⁻¹. The rats were killed 24 or 72 h after a single intraperitoneal injection of C. raciborskii extract in concentrations of 1500, 3000, 6000 and 12,000 μg kg⁻¹ body weight (bw) and an equivalent amount of CYN as present in the highest dose of the extract (79.80 μg CYN kg⁻¹ bw). The genotoxic effect on the livers treated with C. raciborskii was evaluated using comet assay and potential induction of oxidative stress as the toxicity mechanism associated with the presence of CYN in extract. The results from the analyses of DNA damage in the comet tail length, tail moment and percentage of DNA in the tail in the liver indicated that administration of extract and CYN present statistically significant difference when compared with the negative control group. Although an increase in the frequency of selected parameters induced by the CYN was observed in the liver, this damage was less than the damage resulting from the administration of the highest dose of extract. The changes in the biochemical parameters of the hepatic damage showed that the application of single doses of the extract and CYN did not cause serious liver damage in rats. The extract and CYN significantly increased oxidative stress in rats’ liver after a single exposure.

     

Application of the comet assay and detection of DNA damage in haemocytes of medicinal leech affected by aluminium pollution: A case study

This report describes an investigation of genotoxic effects in medicinal leech (Hirudo verbana) exposed to water and sediment of Lake Njivice (Krk Island, Croatia) contaminated by aluminium compounds. The levels of primary DNA damage in leech haemocytes and loss of DNA integrity caused by acute and chronic exposure to contaminated water and sediment were investigated using the alkaline comet assay. Genotoxic effects induced by acute exposure to contaminants were evaluated on leech haemocytes and blood cells of fish and mouse treated ex vivo. The effects of chronic exposure were assessed on haemocytes sampled from an animal kept under laboratory conditions on contaminated water and sediment for 180 days. The results indicate the DNA damaging potential of aluminium compounds present in an excess amount in tested samples.     

Chromosomal aberrations and DNA damage in human populations exposed to the processing of electronics waste

Background, aim, and scope  It has been known that the pollutants of electronic wastes (E-wastes) can lead to severe pollution to the environment. It has been reported that about 50% to 80% of E-wastes from developed countries are exported to Asia and Africa. It has become a major global environmental problem to deal with ‘E-wastes’. E-waste recycling has remained primitive in Jinghai, China. This not only produces enormous environmental pollution but also can bring about toxic or genotoxic effects on the human body, threatening the health of both current residents and future generations living in the local environment. The concentration of lead in the blood of children in the E-waste polluted area in China is higher than that of the control area. But little is known about the cytogenetic effect to human beings caused by the pollution of E-wastes. In the present study, experiments have been performed to investigate the genetics of permanent residents of three villages with numerous E-waste disposal sites and to analyze the harmful effects of exposure to E-wastes. Materials and methods  In total, 171 villagers (exposed group) were randomly selected from permanent residents of three villages located in Jinghai County of Tianjin, China, where there has been massive disposal of E-wastes. Thirty villagers were selected from the neighboring towns without E-waste disposal sites to serve as controls. Chromosomal aberrations and cytokinesis blocking micronucleus were performed to detect the cytogenetic effect, dic + r (dicentric and ring chromosome), monomer, fragments (acentric fragments, minute chromosomes, and acentric rings), translocation, satellite, quadriradial, total aberrations, and micronuclear rate were scored for each subject. DNA damage was detected using comet assay; the DNA percentage in the comet tail (TDNA%), tail moment (TM), and Olive tail moment (OTM) were recorded to describe DNA damage to lymphocytes. Results  The total chromosome aberration rates (5.50%) and micronuclear rates (16.99%) of the exposure group were significantly higher than in the control group (P = 0.000). The percentage of DNA in the comet tail, tail moment, and Olive tail moment detected by comet assay showed that there was a significant difference in DNA damage in the exposure group (P = 0.000). The chromosome aberration, micronucleus rate, and DNA damage observed in women were significantly higher than those in men. Chromosome aberration and micronuclear rates of both smokers and non-smokers in the exposure group are obviously higher than that in the control group (P = 0.000). Discussion  The use of outdated (and unsafe) ways to deal with E-wastes can lead to exposure to a variety of substances harmful to human health. The components of pollution may enter the human body through the air, drinking water, and food chain to damage human genetic material, resulting in genomic instability. The rates of chromosomal aberration, micronucleus formation, and the degree of DNA damage in women in the group exposed to electronic waste were significantly higher than in men. The reason for this may be concerned with the traditional lifestyle of the local residents or the difference of sensitivity to the exposure to E-wastes or any others. Further investigations are needed to provide evidence to demonstrate this. Conclusions  Here, we report the obviously cytogenetic toxicity to the exposure population by the E-waste pollution for the first time. E-waste pollution may be a potential agent of genetic mutation, and may induce cytogenetic damage within the general population exposed to the pollution. These findings need to be considered, and steps should be taken to protect the current population and future generations from the effects of pollution with E-wastes. Recommendations and perspectives  The above results remind us that the impact of E-waste recycling on environmental quality of Jinghai should be evaluated soon. Moreover, it is urgent for the government to prohibit E-waste import and its processing by outdated ways. The future studies such as pollutant details of drinking water, air, and soil in the area as well as epidemiological investigations on the harmful effect to children must be performed eagerly. All the data available do provide a compelling case for immediate action in both countries to address workplace health and safety and waste management. Qiang Liu and Jia Cao contributed equally to this study and share the first authorship.     

Root growth inhibition and induction of DNA damage in soybean (Glycine max) by chlorobenzenes in contaminated soil

The cytotoxic and genotoxic effects of 1,2,4-trichlorobenzene (TCB), chlorobenzene (CB), and hexachlorobenzene (HCB) on root growth and DNA strand breakage damage of soybean nuclei in the test soil were studied using the comet assay. Results indicated that the root growth was significantly inhibited, and DNA strand breaks and the comet tail in the root tip nuclei were both induced after 48 h exposure with TCB concentrations of 50, 100, 200, 300 microg g(-1) in the soil. DNA strand breakage was more sensitive to the TCB than the root growth. There was a significant dose-response relationship between the TCB exposure and DNA strand breakage in the soybean nuclei. Thus it is possible for DNA strand breakage to be used as a biomarker of soybean exposed to TCB contamination. Significant cytotoxic threshold concentration of the TCB exposure on the root growth inhibition was determined as 61 microg g(-1) in the soil. The toxicity of 100-1,000 microg g(-1) CB and HCB to the soybean seedlings in the soil were not observed after 48 h or longer exposure.     

DNA and chromosomal damage induced in fish (Anguilla anguilla L.) by aminomethylphosphonic acid (AMPA)—the major environmental breakdown product of glyphosate

The assessment of the direct impact of breakdown products of pesticide components on aquatic wildlife is ecotoxicologically relevant, but frequently disregarded. In this context, the evaluation of the genotoxic hazard posed by aminomethylphosphonic acid (AMPA—the major natural degradation product of glyphosate) to fish emerges as a critical but unexplored issue. Hence, the main goal of the present research was to assess the AMPA genotoxic potential to fish following short-term exposures (1 and 3 days) to environmentally realistic concentrations (11.8 and 23.6 μg L^?1), using the comet and erythrocytic nuclear abnormalities (ENA) assays, as reflecting different levels of damage, i.e. DNA and chromosomal damage, respectively. Overall, the present findings pointed out the genotoxic hazard of AMPA to fish and, subsequently, the importance of including it in future studies concerning the risk assessment of glyphosate-based herbicides in the water systems.     

Assessing the genotoxic potentials of arsenic in tilapia (Oreochromis mossambicus) using alkaline comet assay and micronucleus test

This experiment was conducted to study the genotoxic potentials of sodium arsenite (NaAsO₂) in freshwater fish Oreochromis mossambicus by using alkaline comet assay and micronucleus (MN) test. Fish were exposed to three different concentrations (3 ppm, 28 ppm and 56 ppm) of arsenic and gill, liver and blood tissue samples were collected after 48 h, 96 h and 192 h of exposure. Arsenic exposure induced DNA damage in all tissues examined in a concentration dependent manner. A significant (p < 0.05) increase in the comet tail DNA (%) of the exposed fish liver, gill, and blood was observed after 48 h and 96 h of exposure, but a decline in DNA damage was recorded in all the tissues at all the three concentrations studied after 192 h of exposure. Liver tissue exhibited significantly (p < 0.05) higher DNA damage at all the concentrations examined, followed by gill and blood. Higher liver tail DNA (51.38 ± 0.21%) refers that it is more prone to injury to arsenic toxicity than the gill and blood. In blood samples arsenic induced micronucleus formation in a concentration dependent manner and highest (5.8 ± 0.46%) value was recorded in 56 ppm after 96 h of exposure, whereas, it was decreased after 192 h of exposure at all the three concentrations of NaAsO₂ examined which refers to the DNA repairing ability of fish to arsenic toxicity. The results of this study depict the genotoxic potentials of arsenic to fish which in turns provide insight on advanced study in aquatic toxicology.     

Genotoxicity in adult residents in mineral coal region—a cross-sectional study

The present study assessed the DNA damage in environmentally exposed volunteers living in seven municipalities in an industrial coal region, through the use of the comet assay with blood cells and the micronucleus test with buccal cells. Blood and buccal smears were collected from 320 male volunteers living in seven cities inserted in a coal region. They were ages of 18 and 50 years and also completed a questionnaire intended to identify factors associated with DNA damage through a Poisson regression analysis. The comet assay detected significant differences in DNA damage in volunteers from different municipalities, and neighboring cities (Pedras Altas, Aceguá, and Hulha Negra) had a higher level of DNA damage in relation to control city. Some of the risk factors associated with identified DNA lesions included residence time and life habits. On the other hand, the micronucleus test did not identify differences between the cities studied, but the regression analysis identified risk factors such as age and life habits (consumption of mate tea and low carbohydrates diet). We conclude that there are differences in the DNA damage of volunteers from different cities of the carboniferous region, but the presence of micronuclei in the oral mucosa does not differ between the same cities. Furthermore, we alert that some related factors may increase the risk of genotoxicity, such as residence location and time, and living and food habits. Finally, we suggest the need for continuous biomonitoring of the population, as well as for investing in health promotion in these vulnerable populations.